Pharmacological models of ADHD

Kostrzewa, Richard M.; Kostrzewa, John P.; Nowak, Przemysław; Brus, Ryszard

doi:10.1007/s00702-007-0826-1

Cited by 53 publications

(23 citation statements)

References 120 publications

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“…This 6-OHDA treatment produces a near-ideal model rodent model of severe Parkinson's disease (Kostrzewa et al 2006). Interestingly, neonatally 6-OHDA-lesioned rats have also been established as a model for attention deficit hyperactivity disorder (ADHD), with adulthood hyperactivity being attenuated by acute amphetamine or methylphenidate treatments (Shaywitz et al 1976;Kostrzewa et al 1994Kostrzewa et al , 2007Davids et al 2003). Histamine too (Liu et al 2008) and manganese (Bouchard et al 2007;Farias et al 2010) also have demonstrated roles in ADHD animal modeling.…”

Section: Discussionmentioning

confidence: 96%

Effect of Pre- and Postnatal Manganese Exposure on Brain Histamine Content in a Rodent Model of Parkinson’s Disease

et al. 2011

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Rats lesioned shortly after birth with 6-hydroxydopamine (6-OHDA; 134 μg icv) represent a near-ideal model of severe Parkinson's disease because of the near-total destruction of nigrostriatal dopaminergic fibers. There are scarce data that in Parkinson's disease, activity of the central histaminergic system is increased. The element manganese, an essential cofactor for many enzymatic reactions, itself in toxic amount, replicates some clinical features similar to those of Parkinson's disease. The aim of this study was to examine the effect of neonatal manganese exposure on 6-OHDA modeling of Parkinson's disease in rats, and to determine effects on histamine content in the brain of these rats in adulthood. Manganese (MnCl₂·4H₂O; 10,000 ppm) was included in the drinking water of pregnant Wistar rats from the time of conception until the 21st day after delivery, the age when neonatal rats were weaned. Control rats consumed tap water. Other groups of neonatal rat pups, on the 3rd day after birth, were pretreated with desipramine (20 mg/kg ip 1 h) prior to bilateral icv administration of 6-OHDA (60 or 134 μg) or its vehicle saline-ascorbic (0.1%) (control). At 2 months after birth, in rats lesioned with 60 or 134 μg 6-OHDA, endogenous striatal dopamine (DA) content was reduced, respectively, by 92 and 98% (HPLC/ED), while co-exposure of these groups to perinatal manganese did not magnify the DA depletion. However, there was prominent enhancement of histamine content in frontal cortex, hippocampus, hypothalamus, and medulla oblongata of adult rat brain after 6-OHDA (60 and 134 μg) injection on the day 3rd postnatal day. These findings indicate that histamine and the central histaminergic system are altered in the brain of rats lesioned to model Parkinson's disease, and that manganese enhances effects of 6-OHDA on histamine in brain.

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Section: Discussionmentioning

confidence: 96%

Effect of Pre- and Postnatal Manganese Exposure on Brain Histamine Content in a Rodent Model of Parkinson’s Disease

et al. 2011

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“…Several animal models of ADHD have been proposed (for review see also Kostrzewa et al 2008;Russell et al 2005;Sagvolden et al 2005;van der Kooij and Glennon 2007), and most of these models were initially based on the presence of hyperactivity. However, face validity of an animal model of ADHD should also include impulsive behaviour and attention deficits.…”

Section: Discussionmentioning

confidence: 99%

Animal models of attention deficit/hyperactivity disorder (ADHD): a critical review

Sontag

Tucha

Walitza

et al. 2010

ADHD Atten Def Hyp Disord

102

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Attention deficit/hyperactivity disorder (ADHD) involves clinically heterogeneous problems including attention deficits, behavioural hyperactivity and impulsivity. Several animal models of ADHD have been proposed, ranging from models with neurotoxic lesions to genetically manipulated animals. An ADHD model is supposed to show phenomenological similarities with the disorder, i.e. it should mimic the three core symptoms (face validity). A model should also conform to an established or hypothesized pathophysiological basis of the disorder (construct validity).Finally, an animal model should be able to predict previously unknown aspects of the neurobiology of ADHD or to provide potential new treatments (predictive validity). The currently proposed models are heterogeneous with regard to their pathophysiological alterations and their ability to mimic behavioural symptoms and to predict response to medication. This might reflect the heterogeneous nature of ADHD. Since the knowledge about the biology of ADHD from human studies is limited, one cannot at present decide which model best represents ADHD or certain ADHD subtypes. Animal models with good face and predictive validity may be useful for investigations of the underlying biological substrates of ADHD. At present, the models in use should be described as animal models of ADHD-like symptoms rather than models of ADHD.

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“…Children who have suffered a brain injury may show some behaviours similar to those of ADHD (Kostrzewa et al 2008). However, this is not likely to be a primary reason because only a small percentage of children with ADHD have suffered a traumatic brain injury.…”

Section: Brain Injuriesmentioning

confidence: 98%

Inflammation: good or bad for ADHD?

Donev

Thome

2010

ADHD Atten Def Hyp Disord

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Attention deficit hyperactivity disorder (ADHD) is characterised by the typical behavioural core symptoms of inattentiveness, hyperactivity and impulsiveness. ADHD is a usually chronic health conditions, mostly diagnosed in childhood, creating a significant challenge for youth, their families and professionals who treat it. This disorder requires long-term treatments, including psychotherapeutic and pharmacological interventions, which in some cases may lead to adverse effects. Understanding the mechanism by which ADHD risk factors affect the biochemical processes in the human brain and consequentially the behaviour will help to identify novel targets for the development of therapeutics with less adverse results and better efficacy including higher responder rates. Although inflammatory responses in the brain have been recognised for years as critical in neurodegeneration and behaviour in a number of neurological and psychiatric disorders, their role for the development, treatment and prevention of ADHD has been so far largely overlooked, although historically, ADHD symptoms were initially observed in patients who survived an ONJ infection, i.e. inflammation. In this review, we discuss the interrelationship between different ADHD risk factors and inflammation with respect to the triggered molecular mechanisms and the contribution they are likely to have to this disorder. This paper provides a rationale for future studies on ADHD with an intent to inspiring the development of new agents for a more efficient management of this disorder.

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Pharmacological models of ADHD

Cited by 53 publications

References 120 publications

Effect of Pre- and Postnatal Manganese Exposure on Brain Histamine Content in a Rodent Model of Parkinson’s Disease

Effect of Pre- and Postnatal Manganese Exposure on Brain Histamine Content in a Rodent Model of Parkinson’s Disease

Animal models of attention deficit/hyperactivity disorder (ADHD): a critical review

Inflammation: good or bad for ADHD?

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